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Pharmacology > chapter 15 CNS > Flashcards

chapter 15 CNS Flashcards

1
Q

use of anorexiants

A
  • prescription weight-loss drugs are used for pt. BMI >30 or BMI>27 with DM, HTN, dyslipidemia
  • serious side effects-cardiac, pulmonary ADRs-possibly fatal
  • avoid in patients with cardiac hx, drug/ETOH abuse
  • difficult to monitor pts with diabetes-increased glucose uptake from skeletal muscles
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2
Q

Anorexiants

A

-for short term use only
-related to amphetamines-suppresses appetite
-Diethylpropion (Tenuate, Tenuate Dospan Cat-IV)
-Orlistat (Xenical, Alli OTC)-only non-stimulant-lipase inhibitor; preg. cat. X
-phentermine (Adepex-P)
-Sibutramine (meridia)
-

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3
Q

pharmacodynamics of anorexiants

A
  • release of norepi/dopamine from storage sites in lateral hypothalmic feeding center
  • decreases appetite
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4
Q

pharmacokinetics of anorexiants

A
  • lipid soluble with wide distribution
  • crosses BBB
  • metabolized by liver and excreted by kidneys
  • duration of action 4-6 yrs
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5
Q

pharmacotherapeutics of anorexiants

A
  • high risk of dependence (avoid pts with ETOH/drug dependence)
  • avoid pt who abuse cocaine/methamphetamines-d/t additional adrenergic stimulation
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6
Q

ADRs for anorexiants

A
  • overstimulation of CNS-agitation, insomnia, dizziness, HTN, etc
  • may cause withdrawal symptoms if suddenly stop
  • increased glucose uptake from skeletal muscles
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7
Q

drug interactions for anorexiants

A
  • off label in combo with SSRI: “Phen-Pro” (prozac and phentermine)
  • with serotonergic meds-blks seratonin production and causes seratonin syndrome (severe muscle rigidity can lead to death)
    • cyproheptadine anecdote
  • MAO inhibitors could lead to HTN crisis
  • lithium toxicity
  • cautious with: adrenergic blks, insulin sulfonylureas, phenothiazines
  • Orlistat decreases level of levothyroxine and increases warfarin
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8
Q

ADHD

A
  • persistent hyperactivity and impulsivity
  • tx: behavior therapy and medication therapy (stimulant and non-stimulant options; used to help with alertness, focus, attention
  • most common drug: MPH (methylphenidate)
  • all stimulants are controlled substance
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9
Q

MPH

A

MAO: blks dopamine reuptake
M: de-esterification to inactive metabolite
AE: insomnia, decreased appetite, weight loss
Rare AE: tics, visual hallucinations
Caution: hx psychosis, mania, drug addiction
DI: carbamazepine, clonidine, warfarin, phenobarb, phenytoin, TCAs
-short and long acting available
* concerta with pt with esophageal motility issues-may increase risk of obstruction

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10
Q

Adderall and Vyvanse

A
  • amphitamines for ADHD
  • ? vyvanse less abuse potential
  • ADRs: decreased appetite, insomnia, abd pn
  • risk of sudden cardiac death
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11
Q

non-stimulant meds for ADHD

A
  • atomoxetine (Strattera)
  • MAO: inhibitor of norepi reuptake
  • metabolized in CYP2D6
  • ADRs: dyspepsia, decreased appetite, wt. loss, no tics
  • can cause severe liver injuries, suicidal ideation
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12
Q

adjunct meds for ADHD

A
  • buproprion
  • clonidine: cautious for sedation
  • TCA: monitor EKG first
  • guafacine: less sedation longer action
  • modanifil-not recommended-hallucinations, Stevens Johnson syndrome
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13
Q

parkinsons disease

A
  • loss of neurons in substantia nigra
  • presence of Lewy bodies
  • loss of dopamine 1 and 2-leading to increased cholinergic activity
  • symptoms: bradykinesia, resting tremor, postural instability
  • progression: depression and psychosis
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14
Q

dopaminergics/dopamine agonist

A
  • choice of tx for parkinson’s
  • attempt to restore functional balance of dopamine and acetylcholine-both responsible for smooth movements and balance
    • either by increasing synthesis, increasing receptors, release from storage, or inactivating MAO leading to more amounts available
      i. e.: amantadine, bromocriptine, levodopa (carbidopa-levodopa), pramipexole, ropinirole
  • many drug intereactions
  • can not stop abruptly
  • cautious with patients with impulse-control disorders (pathologic gambling, binge eating, hypersexuality, excessive shopping etc)
  • “sleep attacks”-suddenly fall asleep
  • confusion and toxic psychosis
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15
Q

cabidopa/levodopa

A

-combination enhances transmission of levodopa across BBB
-levodopa precursor to dopamine
-carbidopa: increases CNS penetration, prevents peripheral dopamine metabolism
ADRs: n/v, arrhythmias, postural hypotension, nightmares
-always given in combination
-absorption: levodopa protein bound, food delays gastric emptying
-controversial when to start tx, enhances neuron degradation, builds dose tolerance

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16
Q

catechol-O-methyltranserase inhibitor (COMT)

A
  • blocks degradation of levodopa
  • entacopone-may have sleep attacks
  • tolcapone-hepatotoxicity-monitor LFTs
  • decreases levodopa requirements
  • adrs: dyskinesias, n/d, discolored urine
17
Q

ergot derivatives for parkinsons

A
  • bromocriptine: limited efficacy, risk of pulmonary fibrosis
  • pergolide: removed from market d/t cardiac valve regurg
18
Q

MAO-B inhibitors for parkinsons

A
  • selegiline, rasagiline
  • inhibits catabolism and reuptake of dopamine
  • can be mono or adjunctive therapy
  • caution with SSRIs, meperidine, tramadol
  • lower dose than for depression
  • adrs: nausea, orthostatic hypotension, may enhance adrs of levodopa
19
Q

anticholinergics for parkinsons

A
  • trihexyphenidyl, benztropine, ethopropazine
  • limited role d/t ADRs
  • used for tremors and drooling
20
Q

drugs associated with seizure activity

A
  • antidepressants: SSRIs, TCA, buproprion
  • quinolones
  • high dose pcn
  • cabepenems
  • theophylline
  • tramadol
  • cyclosporins
  • ETOH, drug, benzo withdrawal
21
Q

anticonvulsants

A
  • seizures are result of abnormal discharge off neurons-anything that disrupts stability of neurons may cause
  • can be used for tx of mood disorders
  • precipitating factors: stress, high intake of caffeine, sleep deprivation, infection, sensory stimuli, hormonal change, metabolic disorders
  • classes: hydantoins, iminostilbenes, succinimides
  • main actions: stimulating influx of chloride ions-assoc. with GABA neurotransmitter
    - delaying influx of Na+
    - delaying influx of Ca+
  • may cause suicide ideation and depression
  • consider levels-toxicity and compliance
  • there are many drug interactions
22
Q

hydantoins

A
  • phenytoin-most commonly used, ethotoin, fosphenytoin
  • inhibit and stabilize electrical discharge in motor cortex of brain
  • first line tx for tonic-clonic and partial complex seizures
23
Q

phenytoin (Dilantin)

A
  • stabilize Na+ channels
  • dose: loading: 15-20mg/kg, maintenance: 4-7mg/kg/day
  • metabolized: non-linear kinetics enzyme inducer
  • many drug interactions
  • caution: hypothyroidism, carbohydrate intolerance, peripheral neuropathy
  • toxicity: n/v, tachycardia,
  • adrs: nystagmus, ataxia, drowsiness, cognitive impairment (dose related)
    • gingival hyperplasia, hirsutism, acne, rash, coarse facial features, osteomalacia, vit D and folic acid deficiency
24
Q

levetiracetam (Keppra)

A
  • for epilepsy and partial seizures/mono or adjunct therapy
  • prevents epileptiform burst firing
  • propagation of seizure activity
  • dose 500mg BID (max of 3g/day)-adjust for renal impairment
  • not largely metabolized-non-hepatic hydrolysis
  • adrs: sedation, fatigue, agitation, lethargy
  • levels: 12-46 mcg/ml
  • pregnancy C
25
Q

iminostilbenes

A
  • used to treat epilepsy, bipolar affective disorder, aggressive behavior, neuralgias
  • carbamazepine (tegretol)
26
Q

carbemazepine (Tegretol)

A
  • structurally related to TCAs
  • inhibits Na+ channels-to prevent seizure activity
  • metabolized by autoinduction-to induce its own metabolism; CYP3A4, 1A2 inducer
    • half life 25-65 hrs decreases to 12-16 hours
      adrs: black box warning blood dyscrasias, rash, ostomalacia, hepatotoxicity, lupus, diplopia, nystagmus
      levels: 4-12 mcg/ml
27
Q

oxcarbazepine

A
  • mono or adjunct therapy for partial seizures
  • Na+ channel blker
  • metabolized in liver: 3A4 inducers, 2C19 inhibitors
    • half life 9 hrs
  • adrs: hyponatremiz, rash, less blood dyscrasias than cabazepine
    levels: 3-35 mcg/ml
  • pregnancy cat C
28
Q

phenobarbital

A
  • for epilepsy low doses to not have dependence or tolerance
  • can be used for tonic-clonic seizures
  • increases aminobutyric acid and chloride influx-causing decrease activity and induce sleep
  • CYP enzyme inducer; half life 80-100 hrs
  • level 15-40 mcg/ml
  • drug interactions: other benzos
  • adrs: faitugue, depression, cognitive impairment, hyperactivity (pediatrics)
  • preg. class D
  • enhanced excretion: urinary alkaline, diuretics
29
Q

valproic acid

A
  • used for primary generalized, absent seizures in adults, myclonic, atonic
  • potentiates GABA, membrane stabilization, K+ channels
  • 10-15 mg/kg/day TID (ER 15% higher)
  • metabolized in liver-1 is hepatotoxic, 10 metabolites, CYP 2C9, 2C19
  • many drug interactions including antacids
  • enzyme inducer
    adrs: GI, derm, wt gain, ataxia, hepatotoxicity, thombocytopenia
  • preg. class D
    levels: 40-100 mcg/ml
30
Q

gabapentin

A
  • inhibits Ca+ channels, enhances GABA
  • 2nd line for partial seizures
  • dose 300-400 mg; titrate, renal dosing
  • can be used for neuropathic pn
    adrs: somnolence, sedation
  • preg. class C
31
Q

pregabalin

A
  • GABA analog; potency>gabapentin
  • used for fibromylagia, postherpetic neuralgia
  • dose: 50 mg TID (max 600 mg/day), renal dose
    adrs: wt. gain, dizziness, somnolent
  • CNS depressant
  • avoid in CHF patients
  • controlled substance
32
Q

succinimides

A
  • treatment of absence seizures in children/adults
  • decreases nerve impulses/transmission in motor cortex leading to higher seizure threshold
  • ethosuximide, mehsuximide
33
Q

ethosuximide

A
  • inhibits Ca+ channels
  • dose: 250 mg BID (max 1.5 g/day)
  • used for absence seizures
  • level: 40-100 mcg/ml
  • metabolized in liver, hepatic hydroxylization, 3A4 involvement
    • excretion through renal and feces
  • half life 60 hrs
  • drug interactions with 3A4 meds
    adrs: GI upset, wt loss, CNS depression, derm, abnormal LFTs, blood dyscrasias
  • preg. class c
34
Q

adjunctive therapies for seizures

A
  • topiramate and zonisamide
  • topiramate-blocks Na+channels, potentiates GABA, blks glutamate, carbonic anhydrase inhibitor; can be used for migraines
  • zonisamide: suppresses focus of seizures via Na+ and Ca+ channels; avoid sulfa allergy,
    adrs: nephrolithiasis
35
Q

migraines

A

3 categories: migraine with aura (classic), without aura (common), complicated migraine-treated by drugs the same

  • patho: vascular theory: aura created by vasoconstriction of intracranial vessels and vasodilation of affected vessels-disproven
    • sertonin: changes cause release of vasoactive neurotransmitter, causes inflammatory response, excitory serotonin receptors activated
  • acute abortive therapy v. prophylactic therapy

Pharmacology (37 decks)

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